Treatment may help asthma sufferers

According to research at Washington University in St. Louis, a two-drug treatment may some day help with restoring healthy breathing in people ill with asthma and chronic bronchitis.

Dr Michael Holtzman and other researchers discovered that some lining cells from the lungs air passages are able to change into another cell type, which leads to the overproduction of mucus in the airways. It was observed in mice and patients suffering from those disorders.

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The researchers think that further testing of the treatments would take not less than a few years, but they claim that the combination of two drugs finally is able to preclude the pernicious transformation of these cells. It would allow the airways to function properly.

Holtzman declared the discoveries are "pushing the rock a little further up the hill" when it comes to apprehension of airway diseases.

He explained that at present doctors prescribe treatments that ease difficulties with breathing, but, unfortunately, those treatments don't influence on mucus production.

Scientists examined mice with a lung condition similar to asthma and chronic obstructive pulmonary disease, a disease classification which includes chronic bronchitis.

They noticed that the airway lining kept an excess of goblet cells (mucus-producing cells) because of a cup-like shape. The number of goblet cells increased as a result of two cellular mechanisms. One mechanism let the cells live longer because of the cilia, small hairs that help remove remains out of the lungs. The other mechanism provoked those cells to change into goblet cells.

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According to Holtzman, in some people an overabundance of goblet cells is noticed because of viral infections or other factors. It leads to particular breathing disorders. He said the scientists proved that the using a combination of two types of inhibitors can block the excess cells.

One slows down the activity of a epidermal growth factor receptor - a type of a protein which is too active on the airway cells with cilia in mice with the asthma-like condition. If the protein was obstructed, the inhibitor precluded the increase of those cells.

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